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PURPOSE: Nitric oxide (NO) may control intraocular pressure (IOP)-regulating mechanisms physiologically and in ocular diseases such as glaucoma. The aim of the present study was to clarify whether an increase in aqueous humor outflow facility could explain the IOP-lowering effect of the NO/cyclic GMP pathway recently described by the authors. METHODS: Test compounds were administered to anesthetized rabbits (New Zealand White, n = 6) intracamerally (5 μl) in the following doses: nitrosocaptopril 12.3 μg, captopril 10.9 μg, sodium nitroprusside (SNP) 13.1 μg, and 8-Br-cGMP 22.3 μg. Outflow facility (C) was determined by the two-level constant pressure infusion method. Outflow facility, C1 and C2, was measured at lower and higher pressure levels, respectively. RESULTS: Outflow facility was increased after treatment with SNP (increase in C in the experimental eye as compared to the control eye C1 80% and C2 74%), nitrosocaptopril (C1 69% and C2 64%) and 8-Br-cGMP (C1 35% and C2 33%). Captopril had no effect on outflow facility (C1 -12% and C2 2%). Blood pressure was not affected by the drugs. CONCLUSIONS: It is concluded that enhancement of outflow facility by nitrosocaptopril, SNP and 8-Br-cGMP, their second messenger derivative, at least partly explains the IOP-lowering effect of NO releasing compounds.
Dr. H. Kotikoski, University of Helsinki, Institute of Biomedicine, Biomedicum Helsinki, Pharmacology, Helsinki, Finland
2.6.2.1 Trabecular meshwork (Part of: 2 Anatomical structures in glaucoma > 2.6 Aqueous humor dynamics > 2.6.2 Outflow)
5 Experimental glaucoma; animal models
11.14 Investigational drugs; pharmacological experiments (Part of: 11 Medical treatment)